Aggressive Coiling of Aortopulmonary Collaterals in Single-Ventricle Patients Is Warranted

Abstract

Aortopulmonary collaterals (APCs) are present in up to 80% of single-ventricle patients undergoing pre-Fontan catheterization [5, 7, 13, 14]. It is theorized that hypoxia is a potent stimulus for the development of APCs [17]. No general consensus exists as to their impact on the midto long-term course of single-ventricle patients. Bradley et al. [2] argued that their presence in the immediate postoperative period after Fontan repair had no impact on the duration of pleural effusions or resource use with regard to length of mechanical ventilation, intensive care unit (ICU), stay, or hospital stay. Although their findings were counterintuitive, even to the authors, this single study has been used as justification to ignore aortopulmonary collaterals not only at the pre-Fontan catheterization but also in the long term at a number of centers (informal polling and personal communication). In the centers performing catheter occlusion of APCs, the criteria for occlusion are subjective and qualitative or based on hemodynamic data that have not been validated in terms of defining what significant APC flow is. Some centers rely on an oxygen step-up from the superior vena cava to branch pulmonary arteries to determine which vessels to occlude in which patients. However, it is clear that many patients would be excluded from catheter occlusion using only this parameter given that collateral flow often enters the lungs distal to the site of sampling. Some centers use filling defects from APC competitive flow noted on pulmonary artery (PA) imaging to discern the degree of negative washout from collaterals (Fig. 1). Some try to gauge the pulsatility of the branch PAs to assess the significance of flow, and some use the PA pressures and end-diastolic pressure measurement of the single ventricle, assuming elevated values are due to volume overloading. Others use the size of APCs, the density of the pulmonary capillary blush (Fig. 2), and opacification of the pulmonary venous return to decide when to occlude. The aforementioned parameters, either singly or in combination, may provide clues as to the volume of collateral flow but can be used only as rough guides. Bradley et al. [2] addressed this issue by quantitating APC flow as the volume of blood returning from the pulmonary venous vent during Fontan surgery [2]. They conceded, however, that their methods were nonphysiologic because flow was measured during hypothermic cardiopulmonary bypass and certainly did not represent a real-life situation. Lim et al. [15] quantitated APC flow using thermal indicator dilution methods in a more physiologic state during the pre-Fontan catheterization, but patients with significant semilunar or atrioventricular valve insufficiency invalidated this technique and were excluded from their study, disqualifying an important subset of patients [10]. In addition, these invasive techniques to evaluate APC flow made it difficult to follow cases in a longitudinal manner. Magnetic resonance imaging (MRI) assessment of PA and pulmonary vein flow using phase-contrast velocity mapping is a promising and accurate noninvasive method for calculating APC flow at the pre-Fontan catheterization and beyond, but it is expensive and time consuming and usually requires general anesthesia [15]. Finally, the long-term impact of permanently occluding vessels off the subclavian arteries and thoracic descending aorta is unknown. A syndrome of chest pain, irritability, and low-grade fevers lasting 3 to 5 days is common after occlusion. Given this backdrop, what is an interventionalist H. J. Stern (&) Cardiology, Stern Cardiology, PC, 4324 Quail View Rd., Charlotte, NC 28226, USA e-mail: tocathu@gmail.com